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大鼠睾丸以及睾丸雌性化雄性(Tfm)大鼠和小鼠睾丸中的促黄体生成素/人绒毛膜促性腺激素反应性腺苷酸环化酶;同源激素引起的脱敏作用

LH/hCG responsive adenylyl cyclase in rat testis and testes from testicular feminized male (Tfm) rats and mice; desensitization by homologous hormone.

作者信息

Hansson V, Jahnsen T, Purvis K, Andersen D, Birnbaumer L

出版信息

Int J Androl. 1980 Dec;3(6):703-12. doi: 10.1111/j.1365-2605.1980.tb00157.x.

Abstract

Testes of testicular feminized (tfm) rats and mice, as well as of normal male rats contain an LH/hCG responsive adenylyl cyclase. Basal, as well as hCG stimulated activities were higher in tfm rats and mice than in normal rats. The presence of an LH/hCG responsive adenylyl cyclase in the testis of tfm rats and mice shows that the greatly elevated LH levels present in males having this syndrome, giving 80-90% reduction in LH/hCG receptors, do not cause an uncoupling of the remaining receptors from the adenylyl cyclase. It also shows that androgens are not essential for coupling of the LH/hCG receptors to the adenylyl cyclase. Injection of 200 IU of hCG into adult normal rats and tfm rats caused, after 48 h, a complete loss of LH/hCG stimulated adenylyl cyclase whereas the FSH responsive adenylyl cyclase in both animal preparations was maintained. Desensitization of the LH responsive adenylyl cyclase by hCG in normal rats, confirms previous studies showing lack of hCG stimulated cyclic-AMP secretion after a comparable dose of hCG in vivo. Similarly, hCG (50 IU) caused a transient loss of LH/hCG responsive adenylyl cyclase in tfm mice, with a complete disappearance of response after 24 h. At 48 and 72 h after injection of hCG the response gradually returned to normal. The fact that hCG caused a complete desensitization of the LH/hCG responsive adenylyl cyclase in both tfm rats and mice, proves that androgen receptor mediated events are not involved in hCG desensitization of the adenylyl cyclase in Leydig cells.

摘要

睾丸雌性化(tfm)大鼠和小鼠以及正常雄性大鼠的睾丸中均含有对促黄体生成素/人绒毛膜促性腺激素(LH/hCG)有反应的腺苷酸环化酶。tfm大鼠和小鼠的基础活性以及hCG刺激的活性均高于正常大鼠。tfm大鼠和小鼠睾丸中存在对LH/hCG有反应的腺苷酸环化酶,这表明患有该综合征的雄性体内LH水平大幅升高,导致LH/hCG受体减少80 - 90%,但并未使剩余受体与腺苷酸环化酶解偶联。这也表明雄激素对于LH/hCG受体与腺苷酸环化酶的偶联并非必不可少。给成年正常大鼠和tfm大鼠注射200国际单位(IU)的hCG,48小时后,LH/hCG刺激的腺苷酸环化酶完全丧失,而两种动物制剂中对促卵泡生成素(FSH)有反应的腺苷酸环化酶则得以维持。正常大鼠中hCG使LH反应性腺苷酸环化酶脱敏,这证实了先前的研究,即在体内给予相当剂量的hCG后,hCG刺激的环磷酸腺苷(cAMP)分泌缺乏。同样,hCG(50 IU)导致tfm小鼠中LH/hCG反应性腺苷酸环化酶短暂丧失,24小时后反应完全消失。注射hCG后48小时和72小时,反应逐渐恢复正常。hCG在tfm大鼠和小鼠中均导致LH/hCG反应性腺苷酸环化酶完全脱敏,这一事实证明雄激素受体介导的事件不参与间质细胞中腺苷酸环化酶的hCG脱敏过程。

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